We have studied the effects of severe constriction of both renal arteries by means of an externally adjustable clamp in conscious dogs instrumented with flowmeters and catheters for serial measurements of cardiac output and arterial pressure. Hypertension produced in this manner regularly caused appearance of malignant hypertension. We found that the malignant phase of renal hypertension can be separated into two different syndromes that are distinguished by 1) their different hemodynamic patterns; 2) the presence or lack of hemolysis in samples of venous blood; and 3) their different responses to treatment with propranolol. One form of malignant hypertension (Type I) was characterized by low cardiac output, the appearance of hemolysis in plasma and responsiveness to treatment with oral propranolol. For reasons not yet clear, it appeared most frequently between April and July; the form (Type II) was associated instead with increased cardiac output, lack of hemolysis and was not responsive to therapy with oral propranolol. Hypokalemia and hyper-reninemia were present to about the same degree in both forms of malignant hypertension and there were about equal increases in blood urea nitrogen and serum creatinine. Histological lesions resembling those of nephrosclerosis in man were found predominantly in the kidneys of Type I malignant hypertension. Not only is the clinical applicability of these observations readily apparent, they form, we believe, the basis of a new approach to determining the etiology of malignant hypertension.